UMEM Educational Pearls - By Mike Winters

Postcardiac Arrest Syndrome: Controlled Reoxygenation

• In previous pearls, Dr. Marcolini has highlighted the poscardiac arrest syndrome (PCAS), comprised of brain injury, myocardial dysfunction, systemic ischemia/reperfusion response, and persistent precipitating disease.
• Not surprisingly, postcardiac arrest brain injury is a major cause of morbidity and mortality, accounting for > 60% of deaths in some studies.
• In addition to therapeutic hypothermia, consider "controlled reoxygenation" in order to optimize neurologic outcome.
• Animal data has demonstrated that too much oxygen may worsen neuronal damage during the initial resuscitation phase.
• Take Home Points:
  • Use a minimum amount of F_iO₂ to maintain S_pO₂ of 94-96%
  • Avoid unnecessary arterial hyperoxia

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PRBC Transfusions in Neurocritical Care

• Historically, neurocritical care textbooks have favored a more liberal PRBC transfusion strategy, as the brain is very sensitive to decreases in oxygen delivery.
• Despite these recommendations, limited studies have failed to show a mortality benefit to PRBC transfusion in critically ill patients with neurologic illness.
• Postulated reasons for the lack of morbidity or mortality benefit center around the injured brain's response to attempts to increase oxygen delivery through transfusion.
  • TBI: PET studies have shown an overall lower level of metabolic activity along with a lower oxygen extraction and loss of autoregulation
  • SAH: transfusion may increase the risk of vasospasm in SAH and worsen flow
• Although the evidence is not overwhelming, current recommendations from SCCM-Eastern Society for the Surgery of Trauma recommend a restrictive PRBC transfusion threshold (Hgb < 7 gm/dL) even in neurocritical care patients.

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PRBC Transfusion Threshold for Patients with Cardiac Disease

• As previously discussed, the PRBC transfusion threshold for the general population of critically ill patients is a Hgb < 7 gm/dL.
• Traditional teaching has been to maintain a Hgb > 10 gm/dL in patients with a history of CAD.
• This threshold stems from a 1950s cohort of Jehovah's Witness patients, and several observational studies, that demonstrated increased perioperative mortality in patients whose Hgb was < 10 gm/dL.
• Recent studies, however, have found that patients with a history of CAD tolerate lower Hgb levels without increases in morbidity or mortality.  In fact, current cardiovascular surgery guidelines favor a conservative Hgb threshold (7 gm/dL) for patients with CAD.
• Importantly, the Hgb threshold of < 7 gm/dL for PRBC transfusion applies to patients with simply a history of CAD and not to patients with evidence of an acute coronary syndrome (STEMI, NSTEMI, unstable angina).  Guidelines continue to recommend a Hgb > 10 gm/dL for patients with ACS.

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Type B Lactic Acidosis

• In the critically ill, patients may often have elevated lactate levels without ongoing tissue hypoperfusion.
• In these patients it is important to consider the causes of what is referred to as "Type B Lactic Acidosis".
• Pertinent to critically ill ED patients, consider the following:
  • Type B1 - related to underlying disease
    • renal faiilure
    • hepatic failure
    • malignancy
    • HIV
  • Type B2 - effects of drugs/toxins
    • acetaminophen
    • alcohols
    • beta-adrenergic agents: epinephrine
    • cocaine, methamphetamine
    • propofol
    • salicylates
    • valproic acid
    • metformin
  • Type B3 - inborn errors of metabolism

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Ventilator Pearls for H1N1 Influenza Virus

• As the spring/summer travel season begins, it is predicted that we will see additional cases of H1N1
• The most common presentation requiring ICU admission to date has been a viral pneumonitis
• As highlighted in previous pearls, the hallmark of disease has been refractory hypoxemia requiring mechanical ventilation in about 85% of patients.
• Current recommendations for H1N1 respiratory failure:
  • Consider early intubation
  • Noninvasive ventilation has been unsuccessful in most and should generally be avoided
  • Low tidal volume settings (6 ml/kg) with PEEP based on F_iO₂ to maintain S_pO₂ > 88% and plateau pressure < 35 cm H₂O
  • Although there is no proven mortality benefit to rescue therapies such as recruitment maneuvers, neuromuscular blockade, and prone ventilation, these can be considered in discussion with your intensivist.

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Warfarin and ICH

• Warfarin causes approximately 10-15% of all intracerebral hemorrhages (ICH)
• Many warfarin-related ICHs occur with INRs in the therapeutic range
• Patients with warfarin-related ICH have higher mortality and typically suffer worse neurologic outcome
• The primary pitfall in treating patients with warfarin-related ICH is the failure to rapidly normalize the INR
• Do not delay treatment while awaiting the results of coagulation labs
• Patients should receive IV vitamin K via slow infusion and FFP
• Prothrombin Complex Concentrate (PCC) is gaining popularity but much of the supporting literature uses agents not available in the US
• Similarly, there is no significant evidence that recombinant factor VIIa improves outcomes in patients with warfarin-related ICH

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Ventilating the Patient with Traumatic Brain Injury

• Many patients with acute TBI will require intubation and mechanical ventilation for a variety of reasons.
• Ventilating the patient with TBI becomes a balancing act between maintaining adequate cerebral perfusion and minimizing lung injury.
• Some pearls to consider:
  • Avoid hypoxia: although guidelines recommend a P_aO₂ > 60 mm Hg, most suggest a higher P_aO₂ (> 80 mm Hg) be initially targeted.
  • Avoid hypercapnia:  many patients will develop hypercapnia when ventilated using the low tidal volume strategy (6 ml/kg) of the ARDSnet trial; titrate TVs to maintain a P_aCO₂ between 32-35 mm Hg.
  • PEEP: the application of PEEP remains controversial in patients with TBI given the theoretical risk of increasing ICP through reductions in venous return; if PEEP is applied pay close attention to the cerebral perfusion pressure to ensure it remains > 60 mm Hg.

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The Rapid Ultrasound in Shock (RUSH) Exam

• Evaluating the ED patient with undifferentiated shock can be challenging.
• Ultrasound can be an invaluable tool in helping to differentiate between hypvolemic, cardiogenic and obstructive shock.
• The RUSH exam essentially focuses on the evaluation of the "pump", the "tank" and the "pipes".
• The pump: exclude pericardial effusion, global estimate of LV EF, and determine if RV strain is present.
• The tank: evaluate the IVC/jugular veins for volume status, look for fluid in the thorax/peritoneum, and exclude pulmonary edema or pneumothorax.
• The pipes: look for a ruptured AAA or aortic dissection and DVT.

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Defining Acute Kidney Injury (AKI)

• In the pearl from 1/5/10, I highlighted the association of AKI with increased morbidity and mortality in the critically ill along with the avoidance of nephrotoxic medications.
• Currently, two sets of criteria (RIFLE and AKIN) can be used to identify patients with AKI
• According to AKIN, the current diagnostic criteria for AKI is:
  • an absolute increase in serum creatinine > 0.3 mg/dL OR
  • a > 50% increase in serum creatinine from patient baseline OR
  • urine output < 0.5 ml/kg/hr for > 6 hours
• For the critically ill ED patient, the most common causes of AKI include sepsis, hypovolemia, medications, trauma, rhabdomyolysis, obstruction and abdominal compartment syndrome

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AKI and the Critically Ill

• Acute kidney injury (AKI) is an abrupt reduction in kidney function causing disturbances in electrolytes, fluids, and acid-base balance.
• AKI occurs in up to 67% of critically ill patients and is associated with a substantial increase in morbidity and mortality.
• AKI in the critically ill is often multifactorial and most commonly due to sepsis, hypovolemia, medications, and hemodynamic instability.
• Medications account for up to 20% of AKI in the critically ill.
• Common medications that cause, or exacerbate AKI, in the critically ill include:
  • NSAIDS
  • Antibiotics (aminoglycosides, amphotericin, acyclovir)
  • ACE-inhibitors
  • Radiocontrast dye
• Take Home Point:  AKI is common in our critically ill ED patients and, whenever possible, avoid nephrotoxic medications that can result in additional injury.

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Appropriate Antimicrobial Therapy for Sepsis

• In previous pearls, we have discussed the importance of early antimicrobial administration for patients with sepsis.
• In patients with septic shock, current guidelines recommend empiric antimicrobial therapy be initiated within 1 hour.
• Equally as important as early administration is the selection of appropriate antimicrobial therapy (i.e. choosing an antibiotic that is effective against the presumed or identified pathogen).
• In one of the most recent studies, investigators found a 5-fold reduction in survival (52% vs. 10.3%) between patients who received appropriate antibiotics compared to those who received antibiotics that were ineffective against the identified pathogen.
• In fact, choosing the right antibiotic is one of the strongest factors associated with patient outcome in sepsis.
• When selecting empiric antimicrobial therapy for patients with septic shock consider patient history, co-morbidities, the clinical site of infection, and local resistance data.

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Early Recognition of Shock

• Early recognition, and thus early treatment, of shock is crucial in reducing morbidity and mortality in the critically ill ED patient.
• Traditionally, the diagnosis of shock has been based on vital sign abnormalities such as tachycardia, tachypnea, oliguria, etc.
• Vital sign abnormalities have been shown to be insensitive markers of shock in the critically ill.
• The Shock Index, although clearly not 100% sensitive, can assist in the detection of shock compared to heart rate and blood pressure alone.
• Shock Index is simply heart rate divided by systolic blood pressure.
• Values greater than 0.9 are abnormal and suggest markedly impaired cardiac output.

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Spinal Epidural Abscess Pitfalls

• The classic triad of back pain, fever, and neurologic deficits are found in < 15% of patients at the time of presentation
• Up to 75% will be afebrile
• Up to 67% will have a normal initial neurologic exam
• < 40% have a WBC greater than 12,000 cells/mm³
• < 33% will have an abnormality on plain film in the first 7-10 days

Take Home Point: In the patient with risk factors for spinal epidural abscess (IVDU, DM, indwelling catheters, etc) do not exclude the diagnosis based upon the absence of a fever, a normal WBC count, and a normal neurologic exam.

Severe Acute Pancreatitis

• Patients with acute pancreatitis are considered to have severe acute pancreatitis (SAP) if they manifest signs of shock, respiratory failure, renal faliure, or GI bleeding.
• SAP is almost universally associated with pulmonary dysfunction, typically manifested as an S_pO₂ < 90% in the first few hours of illness.
• In fact, ARDS develops in at least one-third of patients with SAP.
• Take Home Point: Pay close attention to the patient with acute pancreatitis and a low pulse oximetry reading, as many will rapidly deteriorate from ARDS. In those who deteriorate, early intubation with implementation of lung protective ventilatory strategies is indicated.

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Hypoxemia in the Intubated Asthmatic

• Intubating and mechanically ventilating the asthmatic patient can be frought with potential complications that markedly increase morbidity and mortality.
• In the ventilated asthmatic who develops persistent or worsening hypoxemia, evaluate the patient for the following complications:
  • right main stem intubation
  • pneumothorax
  • ETT displacement
  • ETT obstruction
  • air leak around the ETT
  • gastric distention (decreases respiratory system compliance)
  • ventilator malfunction
  • progressive bronchospasm

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This week's pearl is courtesy of Dr. Evie Marcolini.  Thanks Evie!

Abdominal Compartment Syndrome in Burn Patients

• Patients who receive > 250 ml/kg of fluid in the the 24 hours after burn injury will most likely require abdominal decompression.
• In light of this, bladder pressure monitoring should be part of your practice in resuscitation of the patient with >30% TBSA burns.
• The simple act of placing the bladder probe will increase awareness of the possibility of ACS and prompt measurement of abdominal compartment pressures. 
• ACS can be treated with decompressive laparotomy, or in some cases, percutaneous abdominal decompression.

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Extracorporeal Membrane Oxygenation

• In last week's pearl pertaining to critically ill patients with H1N1, I mentioned the use of ECMO as a potentially life-sustaining treatment for refractory respiratory failure.
• Essentially, ECMO removes blood from the patient and circulates it through an artificial lung with a pump.  For patients with respiratory failure, this is usually accomplished via cannulation of the femoral and internal jugular veins.
• General guidelines to consider ECMO in severe, refractory respiratory failure include:
  • P_aO₂ / F_iO₂ ratio < 100 on 100% F_iO₂ or A-a gradient > 600 mm Hg
  • Age < 65 years
  • No known contraindication to anticoagulation
  • Lack of significant co-morbidities (due to prolonged recovery after weaning from ECMO)

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Critically Ill Patients with H1N1

• Three recent reports published online in the Journal of the Americal Medical Association (JAMA) detail the potential problems of H1N1 infection in the critically ill.
• The three studies (Mexico, Canada, Australia/New Zealand) seem to have recurring themes:
  • shock and multisystem organ failure were common
  • many were healthy, young adults who developed rapid respiratory failure
  • hypoxemia was prolonged and often refractory to conventional modes of mechanical ventilation
• Newer modes of ventilation and therapies were required to treat refractory hypoxemia.  These included high frequency oscillatory ventilation, prone positioning, neuromuscular blockade, nitric oxide, and extracorporeal membrane oxygenation.
• Take Home Point: Involve your intensivist early in the management of ED patients with respiratory failure and suspected H1N1 infection, as non-conventional methods of ventilation may be needed to treat hypoxemia.

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Damage Control Resuscitation

• "Damage control resucitation" is a term that is used to describe the resuscitation strategy of damage control surgical techniques and the tolerance of moderate hypotension, prevention of hypothermia, temporization of acidosis, and the correction of coagulopathy in the severly injured trauma patient.
• In terms of the "lethal triad", it is important to avoid interventions that may cause, or worsen, acidosis.
• A preventable and easily correctable cause of acidosis is hypoventilation.
• In the intubated trauma patient, pay close attention to the minute ventilation to avoid hypoventilation and the accumulation of CO₂.

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Mechanically Ventilated ED Patients and Secretion Mobilization

• As more of our intubated ED patients remain in the ED for longer periods of time, some may develop problems with secretion management (thick/copious amounts of sputum).
• The preferred method of secretion mobilization is heated humidification.
• If you anticipate the duration of intubation to be at least 96 hours, have your respiratory therapist set up a heated humidifier.
• Commonly, clinicians and nurses will instill 5-10 ml of isotonic saline to thin secretions.
• The use of saline to thin secretions is unsupported by the literature and carries a small risk of dislodging the bacterial laden biofilm that covers the endotracheal tube.

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